ReviewMolecular neurobiology1998
Age-related alteration of PKC, a key enzyme in memory processes: physiological and pathological examples.
Review in Molecular neurobiology, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
24 citing papers in PubMed, 75 citations in OpenAlex.
- Bryostatin-1: a promising compound for neurological disorders.Frontiers in pharmacology · 2023Review
- Disruption of a RAC1-centred network is associated with Alzheimer's disease pathology and causes age-dependent neurodegeneration.Human molecular genetics · 2020Article
- Molecular and cellular aspects of age-related cognitive decline and Alzheimer's disease.Behavioural brain research · 2017Review
- The Effects of Phosphatidylserine and Omega-3 Fatty Acid-Containing Supplement on Late Life Depression.Mental illness · 2015Article
- Calcium dysregulation and neuroinflammation: discrete and integrated mechanisms for age-related synaptic dysfunction.Ageing research reviews · 2013Review
- Bryostatin-1 vs. TPPB: dose-dependent APP processing and PKC-α, -δ, and -ε isoform activation in SH-SY5Y neuronal cells.Journal of molecular neuroscience : MN · 2012Article
- Molecular and cellular mechanisms of the age-dependency of opioid analgesia and tolerance.Molecular pain · 2012Review
- The selective inhibition of nuclear PKCζ restores the effectiveness of chemotherapeutic agents in chemoresistant cells.Cell cycle (Georgetown, Tex.) · 2012Article
- Transcriptional regulation of pro-apoptotic protein kinase Cdelta: implications for oxidative stress-induced neuronal cell death.The Journal of biological chemistry · 2011Article
- Development of an in vitro model to evaluate the regenerative capacity of adult brain-derived tyrosine hydroxylase-expressing dopaminergic neurons.Neurochemical research · 2011Article
- Lead-induced accumulation of beta-amyloid in the choroid plexus: role of low density lipoprotein receptor protein-1 and protein kinase C.Neurotoxicology · 2010Article
- Calcium induces expression of cytoplasmic gelsolin in SH-SY5Y and HEK-293 cells.Neurochemical research · 2010Article
- Poststroke neuronal rescue and synaptogenesis mediated in vivo by protein kinase C in adult brains.Proceedings of the National Academy of Sciences of the United States of America · 2008Article
- Expansion of the calcium hypothesis of brain aging and Alzheimer's disease: minding the store.Aging cell · 2007Review
- Differential recruitment of PKC isoforms in HeLa cells during redox stress.Cell stress & chaperones · 2007Article
- Therapeutic effects of PKC activators in Alzheimer's disease transgenic mice.Proceedings of the National Academy of Sciences of the United States of America · 2004Article
- Role of protein kinase Calpha in the regulated secretion of the amyloid precursor protein.Molecular psychiatry · 2003Article
- Dehydroepiandrosterone (DHEA) and the aging brain: flipping a coin in the "fountain of youth".CNS drug reviews · 2003Review
- Protein kinase C activity and the relations between blood lead and neurobehavioral function in lead workers.Environmental health perspectives · 2002Article
- Calcineurin links Ca2+ dysregulation with brain aging.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2001Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Brain aging is characterized by a progressive decline of the cognitive and memory functions. It is becoming increasingly clear that protein phosphorylation and, in particular, the activity of the calcium-phospholipid-dependent protein kinase C (PKC) may be one of the fundamental cellular changes associated with memory function. PKC is a multigene family of enzymes highly expressed in brain tissues. The activation of kinase C is coupled with its translocation from the cytosol to different intracellular sites and recent studies have demonstrated the key role played by several anchoring proteins in this mechanism. PKC-phosphorylating activity appears to be impaired during senescence at brain level in a strain-dependent fashion in rodents. Whereas the levels of the various isoforms do not show age-related alterations, the enzyme translocation upon phorbol-ester treatment is deficitary among all strains investigated. Anchoring proteins may contribute to this activation deficit. We discuss also modifications of the PKC system in Alzheimer's disease that may be related to pathological alterations in neurotransmission. A better insight of the different factors controlling brain-PKC activation may be important not only for elucidating the molecular basis of neuronal transmission, but also for identifying new approaches for correcting or even preventing age-dependent changes in brain function.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.